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With the development of smart grid technology in China, the study of low frequency oscillation early warning has become an important element of power system stability research. Aiming at the problems of single warning indicator with poor accuracy and lack of online warning system in the early warning strategy of low frequency oscillation in power system, a comprehensive low frequency oscillation early warning algorithm based on the evaluation method of kernel matrix hierarchical analysis of fuzzy comprehensive is proposed. Firstly, this method screens out the original data collected by Phasor Measurement Unit (PMU), and extracts the key data volume to form multiple early warning indicators, and generates the trapezoidal fuzzy number judgment matrix. Secondly, by calculating the kernel matrix and consistency test, it is determined whether or not the generated fuzzy matrix is reasonable and calculate the relative weights of the evaluation indicators. The affiliation function is constructed for each early warning indicator. A comprehensive indicator is calculated for multiple indicators, and the reasons of low frequency oscillation in power system are classified by the Random Forest (RF) algorithm. Then, the low-frequency oscillation system is constructed, and the algorithm convergence is proved by the Lyapunov indirect method. The algorithm can automatically determine whether low frequency oscillation occurs or not and classify different types of low frequency oscillations online. Finally, the correctness and validity of this paper's method is verified by a New England 10-machine 39-node system. Compared with the traditional Analytic Hierarchy Process (AHP) method, the proposed method in this paper greatly improves the accuracy of early warning and meets the need of online warning. [ABSTRACT FROM AUTHOR]

Venous thromboembolic complications (VTCs), which include deep vein thrombosis (DVT) and pulmonary embolism (PE), have remained a pressing problem in modern clinical medicine for a long time. Despite the already wide arsenal of modern methods for diagnosing and treating this disease, VTCs rank third in the structure of causes of death among all cardiovascular diseases, behind myocardial infarction (MI) and ischemic stroke (IS). Numerous studies have confirmed the importance of understanding the molecular processes of VTCs for effective therapy and diagnosis. Significant progress has been made in VTC research in recent years, where the relative contribution of microRNAs (miRNAs) in the mechanism of thrombus formation and their consideration as therapeutic targets have been well studied. In this case, accurate, timely, and as early as possible diagnosis of VTCs is of particular importance, which will help improve both short-term and long-term prognoses of patients. This case accounts for the already well-studied circulating miRNAs as non-invasive biomarkers. This study presents currently available literature data on the role of miRNAs in VTCs, revealing their potential as therapeutic targets and diagnostic and prognostic tools for this terrible disease. [ABSTRACT FROM AUTHOR]

Plasma biomarkers are useful tools in the diagnosis and prognosis of heart failure (HF). In the last decade, numerous studies have aimed to identify novel HF biomarkers that would provide superior and/or additional diagnostic, prognostic, or stratification utility. Although numerous biomarkers have been identified, their implementation in clinical practice has so far remained largely unsuccessful. Whereas cardiac-specific biomarkers, including natriuretic peptides (ANP and BNP) and high sensitivity troponins (hsTn), are widely used in clinical practice, other biomarkers have not yet proven their utility. Galectin-3 (Gal-3) and soluble suppression of tumorigenicity 2 (sST2) are the only novel HF biomarkers that are included in the ACC/AHA HF guidelines, but their clinical utility still needs to be demonstrated. In this review, we will describe natriuretic peptides, hsTn, and novel HF biomarkers, including Gal-3, sST2, human epididymis protein 4 (HE4), insulin-like growth factor-binding protein 7 (IGFBP-7), heart fatty acid-binding protein (H-FABP), soluble CD146 (sCD146), interleukin-6 (IL-6), growth differentiation factor 15 (GDF-15), procalcitonin (PCT), adrenomedullin (ADM), microRNAs (miRNAs), and metabolites like 5-oxoproline. We will discuss the biology of these HF biomarkers and conclude that most of them are markers of general pathological processes like fibrosis, cell death, and inflammation, and are not cardiac- or HF-specific. These characteristics explain to a large degree why it has been difficult to relate these biomarkers to a single disease. We propose that, in addition to clinical investigations, it will be pivotal to perform comprehensive preclinical biomarker investigations in animal models of HF in order to fully reveal the potential of these novel HF biomarkers. [ABSTRACT FROM AUTHOR]

Background/Aims: Arsenic trioxide (ATO) is a known anti-acute promyelocytic leukemia (APL) reagent, whose clinical applications are limited by its serious cardiac toxicity and fatal adverse effects, such as sudden cardiac death resulting from long QT syndrome (LQTS). The mechanisms of cardiac arrhythmia due to ATO exposure still need to be elucidated. Long non-coding RNAs (lncRNAs) are emerging as major regulators of various pathophysiological processes. This study aimed to explore the involvement of lncRNAs in ATO-induced LQTS in vivo and in vitro. Methods: For in vivo experiments, mice were administered ATO through the tail vein. For in vitro experiments, ATO was added to the culture medium of primary cultured neonatal mouse cardiomyocytes. To evaluate the effect of lncRNA Kcnq1ot1, siRNA and lentivirus-shRNA were synthesized to knockdown lncRNA Kcnq1ot1.Results: After ATO treatment, the Kcnq1ot1 and Kcnq1 expression levels were down regulated. lncRNA Kcnq1ot1 knockdown prolonged the action potential duration (APD) in vitro and exerted LQTS in vivo. Correspondingly, Kcnq1 expression was decreased after silencing lncRNA Kcnq1ot1. However, the knockdown of Kcnq1 exerted no effect on lncRNA Kcnq1ot1 expression. Conclusions: To our knowledge, this report is the first to demonstrate that lncRNA Kcnq1ot1 downregulation is responsible for QT interval prolongation induced by ATO at least partially by repressing Kcnq1 expression. lncRNA Kcnq1ot1 has important pathophysiological functions in the heart and could become a novel antiarrhythmic target. [ABSTRACT FROM AUTHOR]

We investigated the effect of the incorporation of O atoms into BaSi 2 films on their photoresponse properties. BaSi 2 films with higher O concentration exhibited higher photoresponsivity. Time-of-flight secondary ion mass spectrometry measurements showed that the O atoms were uniformly distributed in the BaSi 2 films, in contrast to our prediction that they would be mostly located around grain boundaries. First-principles calculations revealed that the O atoms occupy the interstitial sites known as the 4 c sites rather than substitutional sites. Moreover, they do not create localized states within the forbidden band gap, which indicates that O atoms incorporated into BaSi 2 are inactive. [ABSTRACT FROM AUTHOR]

Background/Aims: Deregulated myocardial fibrosis is associated with a wide spectrum of cardiac conditions, being considered one of the major causes for heart disease. Our study was designed to investigate the role of microRNA-328 (miR-328) in regulating cardiac fibrosis. Methods: We induced cardiac fibrosis following MI by occlusion of the left coronary artery in C57BL/6 mice. Real-time PCR was employed to evaluate the level of miR-328. Masson’s Trichrome stain was used to evaluate the development of fibrosis. Luciferase activity assay was performed to confirm the miRNA’s binding site in the TGFβRIII gene. Western blot analysis was used to examine TGFβRIII, p-smad2/3 and TGF-β1 at protein level. Results: In this study, we found that miR-328 was significantly upregulated in the border zone of infarcted myocardium of wild type (WT) mice; TGFβRIII was downregulated whereas TGF-β1 was upregulated along with increased cardiac fibrosis. And miR-328 stimulated TGF-β1 signaling and promoted collagen production in cultured fibroblasts. We further found that the pro-fibrotic effect of miR-328 was mediated by targeting TGFβRIII. Additionally, cardiac fibrosis was significantly reduced in infarcted heart when treated with miR-328 antisense. Conclusions: These data suggest that miR-328 is a potent pro-fibrotic miRNA and an important determinant of cardiac fibrosis in diseased heart. [ABSTRACT FROM AUTHOR]

Exploration of impurity elements for carrier density control is important for device application of the BaSi 2 semiconductor, which is a promising candidate for an earth-abundant solar cell absorber. In this study, we have investigated the doping of BaSi 2 films with alkali metals (Li, Na, and K) by deposition of alkali-metal fluorides followed by rapid thermal annealing. Electrical characterization by Hall measurement shows that LiF treatment increases electron density in BaSi 2 up to 10 20 cm − 3 after annealing at 500 °C while NaF and KF treatments have limited effects with electron densities lower than 10 18 cm − 3 . The mechanisms of electrical property modification are discussed from structural viewpoints. Secondary ion mass spectroscopy shows that Li atoms slightly diffuse into the film at 400 °C by prolonged annealing, which nevertheless does not accordingly increase the carrier density. Formation of barium fluoride, oxide, and silicon at 500 °C, which is revealed by energy-dispersive X-ray and Raman spectroscopies, brings about the conclusion that a high temperature is needed for the dissociation of LiF through the reaction with BaSi 2 and the incorporation of Li atoms probably into the interstitial sites of BaSi 2 , which would generate electrons. On the other hand, Na and K atoms are found to evaporate at the same time as the dissociation of NaF and KF, respectively, evidenced by energy-dispersive X-ray spectroscopy. BaF 2 formation accompanied by the NaF dissociation is detected by X-ray diffraction. [ABSTRACT FROM AUTHOR]

Background: Several studies have confirmed the role of microRNAs in regulating ischemia/reperfusion-induced cardiac injury (I/R-I). MiR-17-5p has been regarded as an oncomiR in the development of cancer. However, its potential role in cardiomyocytes has not been exploited. The aim of this study is to investigate the role of miR-17-5p in I/R-I and the underlying mechanism through targeting Stat3, a key surviving factor in cardiomyocytes. Methods: MTT (3-[4, 5-dimethylthiazol-2-yl]-2, 5 diphenyl tetrazolium bromide) assay was used to detect the cell viability. ELISA and TUNEL were performed to measure apoptosis of neonatal rat ventricular cardiomyocytes (NRVCs). Infarct area was estimated by TTC (triphenyltetrazolium chloride) and Evans blue staining. Western blot analysis was employed to detect the Stat3 and p-Stat3 levels and real-time RT-PCR was used to quantify miR-17-5p level. Results: The miR-17-5p level was significantly up-regulated in I/R-I mice and in NRVCs under oxidative stress. Overexpression of miR-17-5p aggravated cardiomyocyte injury with reduced cell viability and enhanced apoptotic cell death induced by H2O2, whereas inhibition of miR-17-5p by its antisense AMO-17-5p abrogated the deleterious changes. Moreover, the locked nucleic acid-modified antisense (LNA-anti-miR-17-5p) markedly decreased the infarct area and apoptosis induced by I/R-I in mice. Furthermore, overexpression of miR-17-5p diminished the p-Stat3 level in response to H2O2. The results from Western blot analysis and luciferase reporter gene assay confirmed Stat3 as a target gene for miR-17-5p. Conclusion: Upregulation of miR-17-5p promotes apoptosis induced by oxidative stress via targeting Stat3, accounting partially for I/R-I. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Three different tunnel junctions (p+-BaSi2/p+-Si, n+-BaSi2/p+-Si and n+-BaSi2/n+-Si) have been fabricated for the formation of BaSi2 solar cells on Si substrates. Investigation of the tunneling properties and surface morphologies of these tunnel junctions has been done to find out which one is the best. From the current-voltage characteristics, p+-BaSi2/p+-Si tunnel junction showed the greatest current of the three. The surface morphologies revealed that the p+-BaSi2/p+-Si tunnel junction has a very smooth surface compared with the other tunnel junctions. Tunnel junction with a smooth surface is a requirement for growing BaSi2 overlayers for BaSi2 solar cells. (© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim) [ABSTRACT FROM AUTHOR]

Long non-coding RNAs (lncRNAs or lncRs) as a new class of regulatory transcripts have been intensively studied for their roles in cardiovascular biology in the past decade. We now know that lncRNAs are significantly implicated in diverse cardiovascular conditions and associated risk factors, including myocardial infarction, coronary heart disease, atherosclerosis/coronary artery disease, vascular disease, cardiac hypertrophy, heart failure, etc. Though in its early stage, research on control of cardiac electrophysiology by lncRNAs has generated some interesting observations and mechanistic insight of significant relevance to translational medicine. This review article focuses on lncRNA regulation of cardiac electrophysiology and arrhythmias with brief discussion on some fundamental aspects of relevant background information for better understanding of the subject. It provides critical analysis of published studies in the literature together with unpublished observations from our own laboratories. In addition to discuss the phenotypes associated with deregulation of lncRNAs, we also try to dissect out the cellular and molecular mechanisms for lncRNAs as regulators of arrhythmogenesis. This review then further touches on the therapeutic implications of lncRNAs and potential strategies for the development of lncRNA-based drugs. Finally, future directions to lncRNA research on cardiac electrophysiology and arrhythmias are anticipated. [ABSTRACT FROM AUTHOR]

In cutaneous wound healing, an overproduction of inflammatory chemokines and bacterial infections impedes the process. Hydrogels can maintain a physiologically moist microenvironment, absorb chemokines, prevent bacterial infection, inhibit bacterial reproduction, and facilitate wound healing at a wound site. The development of hydrogels provides a novel treatment strategy for the entire wound repair process. Here, a series of Fructus Ligustri Lucidi polysaccharide extracts loaded with polyvinyl alcohol (PVA) and pectin hydrogels were successfully fabricated through the freeze–thaw method. A hydrogel containing a 1% mixing weight ratio of FLL-E (named PVA-P-FLL-E1) demonstrated excellent physicochemical properties such as swellability, water retention, degradability, porosity, 00drug release, transparency, and adhesive strength. Notably, this hydrogel exhibited minimal cytotoxicity. Moreover, the crosslinked hydrogel, PVA-P-FLL-E1, displayed multifunctional attributes, including significant antibacterial properties, earlier re-epithelialization, production of few inflammatory cells, the formation of collagen fibers, deposition of collagen I, and faster remodeling of the ECM. Consequently, the PVA-P-FLL-E1 hydrogel stands out as a promising wound dressing due to its superior formulation and enhanced healing effects in wound care. [ABSTRACT FROM AUTHOR]

The valence band structures of a 35-nm-thick BaSi2 epitaxial film on Si(111) have been explored at room temperature by hard x-ray photoelectron spectroscopy (HAXPES). The experimentally obtained photoelectron spectrum is well reproduced by first-principles calculations based on the pseudopotential method. The top of the valence band consists mainly of Si 3s and 3p states in BaSi2, suggesting that the effective mass of holes is small in BaSi2. This is favorable from the viewpoint of solar cell applications. The observed spectrum shifted slightly to the lower energy side due to n-type conductivity of BaSi2. The valence band top was observed at about 0.8 eV below the Fermi level in the HAXPES spectrum. [ABSTRACT FROM AUTHOR]

Phasor Measurement Units (PMU) are capable to generate multi-dimensional time series data, which is one of the most important parts for monitoring power system operation. However, various internal and external factors frequently cause the system to generate anomalous data randomly, so we expect to clean and re-fill the raw PMU data with anomalies to provide support for further advanced applications such as situational awareness, early warning, and dispatch control of the system. Existing methods mostly use classical mathematics and traditional machine learning to analyze PMU data, which makes it difficult to identify the pattern changes of the data under multiple operating conditions in power systems. In this paper, we propose a hybrid model named IRFLMDNN, which consists of an improved CART random forest model and a dynamic neural network optimized by the Levenberg Marquardt algorithm for PMU data anomaly detection and adaptive data re-filling, respectively. Experimental results based on the IEEE 39-node 10-machine New England Power System show that the proposed method has accurate and robust anomaly detection and data refilling performance. [ABSTRACT FROM AUTHOR]

The highest photoresponsivity and an internal quantum efficiency exceeding 70% at 1.55 eV were achieved for 400 nm thick undoped n-type BaSi2 epitaxial layers formed on a n+-BaSi2/p+-Si tunnel junction (TJ) on Si(111). The diffusion of Sb atoms was effectively suppressed by an intermediate polycrystalline Si layer grown by solid phase epitaxy, located between the TJ and undoped BaSi2 layers. [ABSTRACT FROM AUTHOR]

This review outlines the data of numerous studies relating to the broad-spectrum antiviral drug Triazavirin that was launched on the Russian pharmaceutical market in 2014 as an anti-influenza drug (the international non-patented name is Riamilovir). The range of antiviral activity of Triazavirin has been significantly expanded during recent years; in particular, it has been shown that Triazavirin exhibits activity against tick-borne encephalitis, Rift Valley fever, West Nile fever, and other infections of viral etiology. This drug has been approved for treatment of influenza and acute respiratory infections by the Russian Ministry of Health on the basis of comprehensive clinical trials involving over 450 patients. Triazavirin was found to be a highly effective and well-tolerated drug, allowing its over-the-counter sale. The recently published data on the use of Triazavirin in clinical practice for the treatment of patients with COVID-19 are discussed, with special attention paid to potential biological targets for this drug. [ABSTRACT FROM AUTHOR]

Due to the increase in wind power accessing power system in recent years, the low-frequency oscillation of power system is more complicated. Therefore, a new adaptive switching control method combined with a nonlinear system is proposed for the complex operating conditions of the grid-connected power system. Firstly, this method decomposes the low-frequency oscillation control problem of the power system into two parts, which are the linear system control and the nonlinear system control. Then, in the linear system control part, the iterative identification method is used to control this part. In the nonlinear system control part, the nonlinear term is decomposed into a combination of the previous beating measurable and the nonlinear estimation increment. Secondly, the nonlinear system is divided into three different operating conditions by the nonlinear estimation increment. Thus, four different adaptive controllers are obtained. Then, the designed controller is switched according to the controlled object with four controllers by the switching function, which not only ensures the stability of the closed-loop system, but also improves the control performance of the controller under different operating conditions. Finally, the feasibility and effectiveness of this method are verified, and the controller can fit the control efficiency of the real power system well. [ABSTRACT FROM AUTHOR]

Background/Aims: Acute myocardial infarction (AMI) is a devastating cardiovascular disease with a high rate of morbidity and mortality, partly due to enhanced arrhythmogenicity. MicroRNAs (miRNAs) have been shown to participate in the regulation of cardiac ion channels and the associated arrhythmias. The purpose of this study was to test our hypothesis that miR-223-3p contributes to the electrical disorders in AMI via modulating KCND2, the gene encoding voltage-gated channel Kv4.2 that carries transient outward K+ current Ito. Methods: AMI model was established in male Sprague-Dawley (SD) rats by left anterior descending artery (LAD) ligation. Evans blue and TTC staining was used to measure infarct area. Ito was recorded in isolated ventricular cardiomyocytes or cultured neonatal rat ventricular cells (NRVCs) by whole-cell patch-clamp techniques. Western blot analysis was employed to detect the protein level of Kv4.2 and real-time RT-PCR to determine the transcript level of miR-223- 3p. Luciferase assay was used to examine the interaction between miR-223-3p and KCND2 in cultured NRVCs. Results: Expression of miR-223-3p was remarkably upregulated in AMI relative to sham control rats. On the contrary, the protein level of Kv4.2 and Ito density were significantly decreased in AMI. Consistently, transfection of miR-223-3p mimic markedly reduced Kv4.2 protein level and Ito current in cultured NRVCs. Co-transfection of AMO-223-3p (an antisense inhibitor of miR-223-3p) reversed the repressive effect of miR-223-3p. Luciferase assay showed that miR-223-3p, but not the negative control, substantially suppressed the luciferase activity, confirming the direct binding of miR-223-3p to the seed site within the KCND2 sequence. Finally, direct intramuscular injection of AMO-223-3p into the ischemic myocardium to knockdown endogenous miR-223-3p decreased the propensity of ischemic arrhythmias. Conclusions: Upregulation of miR-223-3p in AMI repressed the expression of KCND2/Kv4.2 resulting in reduction of Ito density that can cause APD prolongation and promote arrhythmias in AMI, and therefore knockdown of endogenous miR-223-3p might be considered a new approach for antiarrhythmic therapy of ischemic arrhythmias. [ABSTRACT FROM AUTHOR]

Multidrug‐resistant (MDR) bacterial infection is one of the greatest challenges to public health, a crisis demanding the next generation of highly effective antibacterial agents to specifically target MDR bacteria. Herein, a novel photocatalytic quantum dot (QD)‐armed bacteriophage (QD@Phage) is reported for combating green fluorescent protein‐expressing Pseudomonas aeruginosa (GFP‐P. aeruginosa) infection. The proposed QD@Phage nanosystem not only specifically binds to the host GFP‐P. aeruginosa while preserving the infectivity of the phage itself, but also shows a superior capacity for synergistic bacterial killing by phage and by the photocatalytic localized reactive oxygen species (ROS) generated from anchored QD components. Notably, this highly targeted QD@Phage nanosystem achieves robust in vitro antibacterial elimination for both planktonic (over 99.9%) and biofilm (over 99%) modes of growth. In a mouse wound infection model, this system also shows remarkable activity in eliminating the wound infection and promoting its recovery. These results demonstrate that the novel QD@Phage nanosystem can diversify the existing pool of antibacterial agents and inspire the development of promising therapeutic strategies against MDR bacterial infection. [ABSTRACT FROM AUTHOR]

Estrogen deficiency is associated with increased incidence of cardiovascular diseases. But merely estrogen supplementary treatment can induce many severe complications such as breast cancer. The present study was designed to elucidate molecular mechanisms underlying increased susceptibility of arrhythmogenesis during myocardial infarction with estrogen deprivation, which provides us a new target to cure cardiac disease accompanied with estrogen deprivation. We successfully established a rat model of myocardial ischemia (MI) accompanied with estrogen deprivation by coronary artery ligation and ovariectomy (OVX). Vulnerability and mortality of ventricular arrhythmias increased in estrogen deficiency rats compared to non estrogen deficiency rats when suffered MI, which was associated with down-regulation of microRNA-151-5p (miR-151-5p). Luciferase Reporter Assay demonstrated that miR-151-5p can bind to the 3′-UTR of FXYD1 (coding gene of phospholemman, PLM) and inhibit its expression. We found that the expression of PLM was increased in (OVX+MI) group compared with MI group. More changes such as down-regulation of Kir2.1/IK1, calcium overload had emerged in (OVX+MI) group compared to MI group merely. Transfection of miR-151-5p into primary cultured myocytes decreased PLM levels and [Ca2+]i, however, increased Kir2.1 levels. These effects were abolished by the antisense oligonucleotides against miR-151-5p. Co-immunoprecipitation and immunofluorescent experiments confirmed the co-localization between Kir2.1 and PLM in rat ventricular tissue. We conclude that the increased ventricular arrhythmias vulnerability in response to acute myocardial ischemia in rat is critically dependent upon down-regulation of miR-151-5p. These findings support the proposal that miR-151-5p could be a potential therapeutic target for the prevention of ischemic arrhythmias in the subjects with estrogen deficiency. [ABSTRACT FROM AUTHOR]

Reperfusion stands as a pivotal intervention for ischemic heart disease. However, the restoration of blood flow to ischemic tissue always lead to further damage, which is known as myocardial ischemia/reperfusion injury (MIRI). Ramelteon is an orally administered drug used to improve sleep quality, which is famous for its high bioadaptability and absence of notable addictive characteristics. However, the specific mechanism by which it improves MIRI is still unclear. Sirtuin-3 (Sirt3), primarily located in mitochondria, is crucial in mitigating many cardiac diseases, including MIRI. Based on the structure of Sirt3, we simulated molecular docking and identified several potential amino acid binding sites between it and ramelteon. Therefore, we propose a hypothesis that ramelteon may exert cardioprotective effects by activating the Sirt3 signaling pathway. Our results showed that the activation levels and expression level of Sirt3 were significantly decreased in MIRI tissue and H 2 O 2 stimulated H9C2 cells, while ramelteon treatment upregulated Sirt3 activity and expression. After treat with 3-TYP, a classic Sirt3 activity inhibitor, we constructed myocardial ischemia/reperfusion surgery in vivo and induced H9C2 cells with H 2 O 2 in vitro. The results showed that the myocardial protection and anti-apoptotic effects of ramelteon were antagonized by 3-TYP, indicating that the activation of Sirt3 is a key mechanism for ramelteon to exert myocardial protection. In summary, our results confirm a novel mechanism by which ramelteon improves MIRI by activating Sirt3 signaling pathway, providing strong evidence for the treatment of MIRI with ramelteon. [ABSTRACT FROM AUTHOR]

Nanopatterned poly(3,4-ethylenedioxythiophene):poly(styrenesulfonate) (PEDOT:PSS) layers fabricated by soft-nanoimprint were applied to CH3NH3PbBr3 (MAPbBr3) light-emitting diodes to enhance light extraction. The electric field distribution of MAPbBr3 devices with different periods of the nanopatterned PEDOT:PSS was calculated using the finite-difference time-domain method, demonstrating that the 400-nm period was more effective in improving light outcoupling. By integrating the nanopatterned PEDOT:PSS layer, the external quantum efficiency of the device increased from 6.5% to 10.3%. It can be attributed to the fact that the nanopatterned structure reduced the refractive index discontinuity at the interface between MAPbBr3 and PEDOT:PSS, thereby reducing light trapping in the waveguide mode. [ABSTRACT FROM AUTHOR]

Myocardial infarction (MI)-induced the activation of NLRP3 inflammasome has been well known to aggravate myocardial injury and cardiac dysfunction by causing inflammation and pyroptosis in the heart. Circular RNAs (circRNAs) have been demonstrated to play critical roles in cardiovascular diseases. However, the functions and mechanisms of circRNAs in modulating cardiac inflammatory response and cardiomyocyte pyroptosis remain largely unknown. We revealed that circHelz, a novel circRNA transcribed from the helicase with zinc finger (Helz) gene, was significantly upregulated in both the ischemic myocardium of MI mouse and neonatal mouse ventricular cardiomyocytes (NMVCs) exposed to hypoxia. Overexpression of circHelz caused cardiomyocyte injury in NMVCs by activating the NLRP3 inflammasome and inducing pyroptosis, while circHelz silencing reduced these effects induced by hypoxia. Furthermore, knockdown of circHelz remarkably attenuated NLRP3 expression, decreased myocardial infarct size, pyroptosis, inflammation, and increased cardiac function in vivo after MI. Overexpression of miR-133a-3p in cardiomyocytes greatly prevented pyroptosis in the presence of hypoxia or circHelz by targeting NLRP3 in NMVCs. Mechanistically, circHelz functioned as an endogenous sponge for miR-133a-3p via suppressing its activity. Overall, our results demonstrate that circHelz causes myocardial injury by triggering the NLRP3 inflammasome-mediated pro-inflammatory response and subsequent pyroptosis in cardiomyocytes by inhibiting miR-133a-3p function. Therefore, interfering with circHelz/miR-133a-3p/NLRP3 axis might be a promising therapeutic approach for ischemic cardiac diseases. Underlying mechanisms of circHelz in the regulation of myocardial infarction. [Display omitted] • Silencing CircHelz improves cardiac function and decreases infarct size post-AMI. • CircHelz leads to cardiomyocyte injury by activating NLRP3 inflammasome induced pyroptosis. • CircHelz reduces miR-133a-3p activity by acting as its endogenous sponge. • CircHelz/miR-133a/NLRP3 is a novel therapeutic target for ischemic heart disease. [ABSTRACT FROM AUTHOR]

In this work, a new narrow bandpass filter based on double-layer metallic woven meshes (MWMs) is experimental and numerically investigated. Differing from generally reported 2D planar structures, the MWM is a 3D structure consisting of metal cross-bending wires. Multiple resonant peaks with high isolation originating from the Fabry-Perot cavities are achieved by changing the distance between two MWM layers. Simulated results show that an optimized double-layer MWMs presented a sharp resonant peak whose full width at half maximum is narrower than 1.25 GHz. The achievement of such filters based on the engineered Fabry-Perot cavity would provide a new method for the design of ultra-narrowband filters and ultra-sensitive sensors in terahertz regions. • An ultra-narrow bandpass filter based on double-layer metallic woven meshes (MWMs) is investigated. • The woven mesh is a 3D structure consisting of metal cross-bending wires. • Multiple resonant peaks with high isolation originating from the 3D Fabry-Perot cavities are achieved. • A sharp resonant peak whose full width at half maximum is narrower than 1.25 GHz is achieved. • This achievement would provide a new method for the design of ultra-narrowband filters in terahertz regions. [ABSTRACT FROM AUTHOR]

MXene layered nanochannels are assembled into a sandwich structure of Ag/MXene/H 3 PO 4 -PVA/Ag, in which a weak interaction of hydrogen bond is created between H+ ions and the hydroxyl (OH) termination of MXene surface during the pseudo-intercalation of H+ ions. As a result, the hydrogen bond leads to the trapping and hysteretic transport of H+ ions, which triggers the memcapacitance effect. [Display omitted] • Two-dimensional MXene nanosheets with rich surface chemistry are assembled into the layered nanochannels. • A sandwich structure of Ag/MXene/H 3 PO 4 -PVA/Ag exhibits the promising memcapacitance effect. • A weak interaction of hydrogen bond is created between H+ ions and the hydroxyl (OH) termination of MXene surface. • The hydrogen bond leads to the trapping and hysteretic transport of H+ ions, triggering the memcapacitance effect. Two-dimensional materials provide an unprecedented opportunity to fabricate ion nanochannels for exploring memcapacitance. However, the full understanding of ion transport remains vague due to complex interfacial reactions and potential interactions between ions and nanochannels. Herein, a sandwich structure of Ag/MXene/H 3 PO 4 -PVA/Ag with MXene layered nanochannels exhibits the promising memcapacitance effect. Through investigating the interfacial electrochemical information, it is found that a weak interaction of hydrogen bond is created between H+ ions and the hydroxyl (OH) termination of MXene surface during the pseudo-intercalation of H+ ions. As a result, the hydrogen bond leads to the trapping and hysteretic transport of H+ ions, which triggers the memcapacitance effect. This work demonstrates that 2D materials with rich surface chemistry could be selected as a promising candidate for constructing ion nanochannels for creating novel nanoionic devices. [ABSTRACT FROM AUTHOR]

SF 6 /N 2 mixtures is considered as a practical alternative proposal of SF 6 in GIS and GIL. Simulating particle transportations and chemical reactions during the positive streamer propagation in SF 6 /N 2 mixtures assists in the insulation performance optimization of SF 6 /N 2 mixtures. This paper presents a fluid dynamic model coupled with the chemical reaction system for the positive streamer propagation in SF 6 /N 2 mixtures. The Townsend coefficients of the 20%SF 6 /80%N 2 mixture derived from the proposed chemical reaction system are in accordance with the measurement results. Based on this model, the propagation of the positive streamer in a 1 mm needle-plate gap in the 20%SF 6 /80%N 2 mixture is simulated. Simulated results indicate that there exists a negative space charge region in the streamer channel. It can be attributed to the increasing attachment rates of SF 6 yielding SF 5 − and SF 6 −, and the reduction of the ionization rates of N 2 and SF 6 in the streamer channel. Besides, it is noted that the ionization activities of N 2 and SF 6 at the streamer head are equally important to support the continuous propagation of the positive streamer. The ionization of N 2 in the streamer channel serves as an important factor to supply electrons and avoid the accumulation of the negative space charge. [ABSTRACT FROM AUTHOR]

A mutant generated via ethylmethane sulfonate mutagenesis, Desmodesmus sp. G3, exhibited greater biomass and neutral lipid production over the wild type (WT) strain Desmodesmus sp. G41 in our previous study (Zhang et al., Bioresour Technol 207:268–275, 2016). G3 possessed a higher growth rate and lipid production than WT, with a biomass yield and total lipid content of 1302.86 mg L−1 and 48.58% respectively, which was promoted by 20.50% and 18.84%, compared to WT. Comparative transcriptome analysis was performed to elucidate the mechanism supporting enhanced biomass and lipid production in G3. A total of 1488 differentially expressed genes (DEGs) was identified comparing G3 and WT sequencing datasets, of which 753 and 735 genes were upregulated and downregulated respectively in G3. Pathway enrichment analysis indicated that 'photosynthesis,' 'starch and sucrose metabolism,' 'fatty acid elongation,' and 'pyruvate metabolism' were the notable represented DEGs-enriched pathways that might affect cell growth and lipid metabolism. Light harvesting capture was enhanced in G3. To protect PSII from photodamage, light harvesting complex-dependent non-photochemical quenching and state transitions was employed as the photoprotective strategy. De novo fatty acids (FAs) synthesis in chloroplast was downregulated in G3 while mitochondrion localized FAs elongation was enhanced to recycle carbon skeletons for lipid biosynthesis. Pyruvate mechanism was activated in G3 to generate acetyl-CoA through a pyruvate dehydrogenase bypass pathway, as the predominant pathway to provide precursor for lipids biosynthesis. [ABSTRACT FROM AUTHOR]

• We prepared highly conductive, highly transparent amorphous IWO films. • The efficiency of ST-PSCs was nearly identical to that of opaque cells. • RPD can be used to deposit IWO on Spiro-OMeTAD without any protective layer. A low-damage approach to fabricate high-quality W-doped In 2 O 3 (IWO) films as transparent electrodes for semi-transparent perovskite solar cells was developed by the use of a reactive plasma deposition (RPD) equipment. IWO films were directly deposited on Spiro-OMeTAD by RPD at room temperature. The high O 2 flux can be effectively reduce the resistance at the IWO/Spiro-OMeTAD interface, resulting in the improved solar cell performance. The maximum efficiency of the IWO-based perovskite solar cells was 16.5%, comparable to that of conventional Ag electrode solar cells. This demonstrates that the deposition of TCO-based electrodes without protective buffer layers is available by RPD. [ABSTRACT FROM AUTHOR]

Abstract An n-type Si nanowire (SiNW) solar cell based on transition metal oxides V 2 O 5 and TiO 2 has been fabricated. The cell is demonstrated in the ITO/V 2 O 5 /n-SiNWs/TiO 2 /Al heterojunction structure, in which the V 2 O 5 and TiO 2 work as the hole- and the electron-selective layers, respectively. Parameters of cells with different lengths of nanowires have been investigated. Owing to the excellent light trapping effect of nanowire arrays and superior carrier transporting properties of thin V 2 O 5 and TiO 2 layers, an improved power conversion efficiency of 12.7% has been achieved in a cell with 1.45-μm-long nanowires. Due to the large work function difference between V 2 O 5 and n-Si, a build-in potential of 0.75 V was obtained from the capacitance-voltage measurement, which implies the possibility of achieving a large open circuit voltage for these nanowire solar cells. The efficiency loss is mainly caused by the recombination via the defects on the unpassivated surface of SiNWs. By solving this problem, the cell efficiency may be improved further and realize the application in PV industries. Highlights • The first study to apply transition metal oxides to form Si nanowire solar cells. • Obtaining a large build-in potential by the high work function V 2 O 5 layer. • The large J SC obtained by the light trapping of nanowires boosts the efficiency. • The formation process of this solar cell is cost-effective and easily manufactured. [ABSTRACT FROM AUTHOR]

W-doped In 2 O 3 (IWO) films prepared by reactive plasma deposition (RPD) technique at 150 °C have been studied to replace Sn-doped In 2 O 3 (ITO) serving as transparent electrodes for p-i-n structured perovskite solar cells. The optical and electrical properties of IWO films were found to depend on the oxygen partial pressure of deposition process. Compared with the reference ITO films, the IWO films obtained at an oxygen partial pressure of 0.12 Pa exhibited prominent performance, including higher near-infrared transmittance and carrier mobility. Furthermore, the IWO films showed higher work function than that of the ITO films, resulting in the enhancement of open-circuit voltage (0.982 V vs 0.901 V) and conversion efficiency (12.9 % vs 11.9 %). It can be attributed to that high work function of the IWO films reduced the carrier transport barrier at the interface between transparent electrode and PEDOT:PSS and enhanced the carrier collection near the edge of the perovskite bandgap. The excellent properties of the RPD-prepared IWO films indicate that it is a promising transparent electrode material for p-i-n structured perovskite solar cells, especially for applications requiring low-temperature fabrication. • IWO films fabricated by RPD method at 150 °C were developed and applied to p-i-n structured perovskite solar cells. • Compared with the reference ITO films, the IWO films showed higher near-infrared transmittance and carrier mobility. • The IWO film exhibited a higher work function than the reference ITO film, leading to improved V oc of perovskite solar cells. • The conversion efficiency of IWO-based solar cells was higher than that of ITO-based solar cells (12.9 % vs 11.9 %). [ABSTRACT FROM AUTHOR]

Abstract: Cardiac hypertrophy is a primary predictor of progressive heart disease that often results in heart failure. Growing evidence has demonstrated that microRNAs (miRNAs) play a critical role in regulating cardiac hypertrophy. This study was designed to evaluate the effect of miR-328 on cardiac hypertrophy and the potential molecular mechanisms. We found that transgenic overexpression of miR-328 in the heart induced cardiac hypertrophy in mice, which was accompanied by reduced SERCA2a level increased intracellular calcium concentration and calcineurin protein level, and enhanced NFATc3 nuclear translocation. However, normalization of miR-328 level by its antisense chemically modified with locked nucleic acid (LNA-antimiR-328) reversed the changes. Forced expression of miR-328 resulted in cardiomyocyte hypertrophy in cultured neonatal rat ventricular cells, which was accompanied by downregulation of SERCA2a expression and activation of the calcineurin/NFATc3 signaling pathway. These changes were abolished by LNA-antimiR-328. We validated the SERCA2a as a direct target for miR-328. MiR-328 expression was upregulated in cardiomyocyte treated with isoproterenol (ISO) to induce hypertrophy; while knockdown of miR-328 attenuated the hypertrophic responses. The level of miR-328 was significantly elevated in a mouse model of hypertrophy by thoracic aortic banding (TAC). Consistently, SERCA2a was downregulated, whereas calcineurin were upregulated, and NFATc3 nuclear translocation was enhanced. In contrast, hypertrophy in these mice was significantly alleviated when treated with miR-328 antisense. MiR-328 promotes cardiac hypertrophy by targeting SERCA2a. Our study therefore uncovered a novel molecular mechanism for cardiac hypertrophy and indicated miR-328 as a potential therapeutic target for this cardiac condition. [Copyright &y& Elsevier]

Abstract: We have successfully grown a-axis-oriented p-type BaSi2 films on Si(111) by in situ boron (B) doping using molecular beam epitaxy (MBE). The hole concentration in B-doped BaSi2 was controlled in the range between 1017 and 1019 cm−3 at room temperature by changing the temperature of the B Knudsen cell crucible. The acceptor level was estimated to be approximately 23meV. [Copyright &y& Elsevier]

Myocardial fibrosis in post-myocardial infarction is a self-healing process of the myocardium, making ventricular remodelling difficult to reverse and develop continuously. Fibroblast growth factor 21 (FGF21) plays an essential role in cardiovascular and metabolic diseases. However, the effect and mechanism of FGF21 action on cardiac inflammation and fibrosis caused by myocardial injury have rarely been reported. Adult male Sprague–Dawley rats administered with or without recombinant human basic FGF21 (rhbFGF21) were assessed using echocardiography and haematoxylin-eosin and Masson's trichrome staining to determine the cardiac function and cardiac inflammation and fibrosis levels. FGF21 might improve cardiac remodelling, as characterised by a decrease in the expression of a series of inflammatory and fibrosis-related factors. Moreover, when FGF receptors (FGFRs) were blocked, the effects of FGF21 disappeared. Mechanistically, we found that oxidative stress induced the downregulation of early growth response protein 1 (EGR1), which contributed to inflammatory factors and fibrosis reduction in cardiomyocytes treated with H 2 O 2. Collectively, FGF21 effectively suppressed the inflammation and fibrosis in post-infarcted hearts by regulating FGFR-EGR1. Fibroblast growth factor 21 (FGF21) alleviated fibrosis and inflammatory reaction induced by myocardial infarction via the FGFR-EGR1 signal pathway. [Display omitted] • Fibroblast growth factor 21 (FGF21) effectively suppressed inflammation and fibrosis in post-infarcted hearts. • Early growth response protein 1 (EGR1) participated in inflammation and fibrosis in post-infarcted hearts. • The mechanisms of FGF21's anti-inflammation and anti-fibrosis are closely related to transcriptional regulation. [ABSTRACT FROM AUTHOR]

Mn-doped CsPbCl 3 nanocrystals are considered to be a promising material for luminescence and display applications owing to Mn doping provides a way to introduce new optical properties and reduce the use of toxic Pb. Complicate ion-exchange and hot-injection are commonly used for the fabrication of the nanocrystals. Developing a fast and efficient synthesis method remains a challenge so far. Herein, we developed a simplified solid-state mechanochemical approach to synthesize Mn-doped CsPbCl 3 nanocrystals and investigated the structure and luminescence properties of the as-synthesized nanocrystals. Cubic morphology of Mn-doped CsPbCl 3 nanocrystals with average size of 13 nm have been obtained by this approach. Mn was successfully incorporated in CsPbCl 3 perovskite nanocrystals, resulting in a high photoluminescence quantum yield of 40.7% with an improvement of stability. Emission peak of 594 nm that can be assigned to the luminescence of Mn2+ d-d transition was observed under 365 nm UV excitation. The color of the luminescence changed from blue to warm white to yellow depended on the amount of Mn doping, exhibiting a tunable-color property. It is expected that this approach provides an effective route that would help for synthesis of perovskite nanocrystals doped with different dopants. Mn-doped CsPbCl 3 nanocrystals fabricated by a solid-state mechanochemical synthesis exhibit tunable color and a high photoluminescence quantum yield of 40.7%. Image 1 • Mn-doped CsPbCl 3 nanocrystals were synthesized by a solid-state mechanochemical approach for the first time. • Cubic morphology of Mn-doped CsPbCl 3 nanocrystals with an average size of 13 nm were obtained. • Doping of Mn increased the photoluminescence quantum yield to 40.7% and enhanced the stability of CsPbCl 3 nanocrystals. • Tunable photoluminescence color was achieved by regulating the Mn content in CsPbCl 3 nanocrystals. [ABSTRACT FROM AUTHOR]

• We for the first time investigated that Melatonin exerted anti-tumor activities in Hodgkin lymphoma via inhibiting cell proliferation and promoting cell apoptosis. • Melatonin treatment induced autophagy in Hodgkin lymphoma cells. • Melatonin induces autophagy by increasing the expression of RORC. Melatonin (Mel) has been shown to involve in many essential cell functions via modulating many signaling pathways. We for the first time investigated that Mel exerted anti-tumor activities in Hodgkin lymphoma (HL) via inhibiting cell proliferation and promoting cell apoptosis. Further study revealed that Mel treatment increased expression of LC3-II and decreased p62 proteins with the enhanced production of autolysosome, indicating it induced activation of autophagy. Nevertheless, Mel treatment together with autophagy inhibitors 3-MA or CQ exacerbated the damage effect of Mel in HL cells, which means autophagy plays a protective role in this process. Furthermore, we found Mel treatment increased the expression of G protein-coupled receptors MT2 and retinoic acid-related orphan receptors (RORs), eg. RORA, RORB and RORC. While RORC has the highest increase in Mel treated HL cells. In addition, RORC overexpression induced autophagy activation. Therefore, Mel showed tumor-suppressive role due to an increased level of RORC induced autophagy in HL. [ABSTRACT FROM AUTHOR]

• Cardiomyocyte contributes to elevation of Dectin-1 expression post-MI. • Silencing Dectin-1 improves cardiac remodeling and function in the ischemic heart. • Dectin-1 aggravates MI induced cardiac dysfunction by partially activating NF- κ B/NLRP3 axis. The myocardial inflammatory response is a consequence of myocardial infarction (MI), which may deteriorate cardiac remodeling and lead to dysfunction in the heart post-MI. Dectin-1 is a c-type lectin, which has been shown to regulate innate immune responses to pathogens. However, the role of Dectin-1 in the heart diseases remains largely unknown. In this study, we aimed to investigate the effects of Dectin-1 on cardiac remodeling post-MI. We found that cardiac Dectin-1 mRNA and protein expressions were significantly elevated in C57BL/6 mice after MI. In vitro , hypoxia induced cardiomyocyte injury in parallel with increased Dectin-1 protein expression. Knockdown of Dectin-1 remarkably attenuated cardiomyocyte death under hypoxia and lipopolysaccharide (LPS) stimulation. In vivo administration of adeno-associated virus serotype 9 mediated silencing of Dectin-1, which significantly decreased cardiac fibrosis, dilatation, and improved cardiac function in the mice post-MI. At the molecular level, downregulation of Dectin-1 dramatically suppressed up-regulation of nuclear factor-κB (NF-κB), nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), and the inflammatory genes involved in fibrogenesis and cardiac remodeling after MI. Furthermore, treatment with BAY11-7082, an inhibitor of NF-κB, repressed the activation of NF-κB, and attenuated LPS induced elevation of NLRP3 and cell death in cardiomyocytes. Collectively, upregulation of Dectin-1 in cardiomyocytes post-MI contributes to cardiac remodeling and cardiac dysfunction at least partially by activating NF-κB and NLRP3. This study identified Dectin-1 as a promising therapeutic target for ischemic heart disease. [ABSTRACT FROM AUTHOR]

• The first study to apply pulsed laser deposition on growing BaSi 2 thin films. • Poly-BaSi 2 thin films with a large absorption coefficient are achieved. • The PLD-deposited BaSi 2 thin films keep a good stoichiometric ratio close to 1:2. A new growth method for BaSi 2 thin films by using pulsed laser deposition (PLD) on transparent SiO 2 and CaF 2 substrates has been developed. X-ray diffraction and Raman spectroscopy revealed the poly-crystalline property of the deposited films. By introducing a thin Si buffer layer on the SiO 2 substrate, the crystalline quality of BaSi 2 thin films were improved. BaSi 2 thin films exhibited a Ba/Si ratio very close to 0.5, indicating the good stoichiometry control of PLD growth. The absorption coefficient of the poly-BaSi 2 thin film reached 105 cm−1 and its band gap was deduced to be 1.32 eV, which are similar to those grown by molecular beam epitaxy or sputtering. A maximum photoresponsivity of 12.5 mA/W was achieved in the BaSi 2 thin film, which implies the potential of PLD-deposited BaSi 2 for thin film solar cell applications. [ABSTRACT FROM AUTHOR]